Pediatric emergency medicine trisk 4566 4566
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(including ptosis) progressing to flaccid paralysis. Nicotinic effects on
sympathetic activity may also result in tachycardia, hypertension, and metabolic
aberrations (e.g., hyperglycemia, hypokalemia, metabolic acidosis). Muscarinic
toxicity is manifested by ocular findings (miosis, visual blurring, eye pain,
lacrimation), respiratory distress (watery rhinorrhea, bronchospasm, increased
bronchial secretions causing cough, wheezing, dyspnea), dermal involvement
(flushing, sweating, cyanosis), GI signs and symptoms (salivation, nausea,
vomiting, diarrhea progressing to fecal incontinence and abdominal cramps),
genitourinary complaints (frequency, urgency, incontinence), and cardiovascular
findings (bradycardia, hypotension, atrioventricular block). Because muscarinic
effects on the heart are opposed by the cardiovascular effects of nicotinic
hyperstimulation at autonomic ganglia, heart rate and blood pressure may be
either elevated or depressed and are not reliable indicators of the severity of
nerve-agent intoxication.
Clinical Presentation. The clinical presentation in a given patient depends on
dose and route of exposure. For vapor exposures, mild toxicity would be
suggested by miosis, rhinorrhea, mild dyspnea, and wheezing—all local effects
caused by contact of vapor with epithelial surfaces. As the dose increases and
systemic distribution of the agent occurs, the victim might experience increased
respiratory secretions and dyspnea, nausea, vomiting, and muscle weakness. In
the Tokyo experience with sarin vapor exposure, miosis (99%), dyspnea (63%),
nausea (60%), and headache (74%) were particularly common among moderately
symptomatic patients at hospital admission. In severe cases with exposure to high
vapor concentrations, paralysis, and seizures leading to death from respiratory
arrest may occur within minutes and sometimes nearly instantaneously. In the
Tokyo incident, 3 of 640 patients presented to one ED in cardiopulmonary arrest.
The asymptomatic period between exposure and the onset of signs and
symptoms is termed the latent period. It is important to stress two aspects of this
concept with respect to nerve agents: First, the onset of clinical effects is
immediate or nearly immediate after the inhalation of a substantial dose of vapor,
whereas there is a delay after skin exposure. This is because it takes time for
nerve agent to pass through the stratum corneum (where it forms a temporary
depot) and reach the dermal capillaries for introduction into the systemic
circulation. Second, the length of the latent period, whether for inhalation or
dermal exposure, is inversely correlated with dose. For example, a very small
drop of VX applied to the skin may cause rapid local effects (localized sweating
and then fasciculations of underlying muscle fibers) but may take up to 18 hours
